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Mechanisms of tolerance induction: blockade of co-stimulation Sebille F; Vanhove B; Soulillou JPPhilos Trans R Soc Lond B Biol Sci 2001[May]; 356 (1409): 649-57Induction of tolerance to transplantation antigens is believed to be a promising way to achieve long-term allograft survival without a deleterious immunosuppressive regimen. T-cell activation, which is an essential feature of graft rejection, requires a first signal provided by T-cell receptor (TCR) ligation and a second signal provided by engagement of co-stimulatory molecules with their respective ligands on antigen-presenting cells. The coordinated triggering of these two independent signalling systems ensures the full T-cell activation, including proliferation and acquisition of effector function. TCR occupancy in the absence of co-stimulatory signals leads to a sustained loss of antigen responsiveness called clonal anergy, which could be of major importance in transplantation. In vivo, co-stimulation blockade was indeed shown to allow for long-term allograft survival in several transplantation models. However, the current continuous identification of new co-stimulatory molecules suggests that a functional redundancy of the system exists and that tolerance to transplantation antigens might be achieved more easily through the combined blockade of two or several co-stimulatory signals. In this review, we analyse the biological effects of the disruption of some co-stimulation pathways in vitro and in vivo and discuss their potential interest for tolerance induction.|Animals[MESH]|B7-1 Antigen/*immunology[MESH]|CD2 Antigens/*immunology[MESH]|CD28 Antigens/*immunology[MESH]|CD40 Antigens/*immunology[MESH]|CD40 Ligand/*immunology[MESH]|Humans[MESH]|Lymphocyte Function-Associated Antigen-1/*immunology[MESH]|Transplantation Tolerance/*immunology[MESH] |
